Correction of fragile X syndrome in mice.

By Gül Dölen, Emily K. Osterweil, B. Rao, Gordon B. Smith, Benjamin D. Auerbach, Sumantra Chattarji, Mark F. Bear. Neuron, 2007

984 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/201f0c8b08ddd03ed6121f3d48b1fcd993e19e6d

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Citations in the corpus

A synaptic trek to autism. (2009, background): “Similarly, abnormal synaptic functions could be reversed in adult mice model for fragile X or Rett syndrome [45 ,46,47].”
The autistic neuron: troubled translation? (2008, background): “This 35, October 31, 2008 ©2008 Elsevier Inc. 403 phenotype has been observed in Fmr1 knockout mice (Dolen et al., 2007).”
Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132. (2010, neutral): “LTP is abolished in cortex and amygdala (but not hippocampus), the threshold for spike-timing-dependent plasticity is increased, and ocular dominance plasticity is altered (Desai et al., 2006; Dolen et al., 2007; Li et al., 2002; Meredith et al., 2007; Zhao et al., 2005).”
Metabotropic glutamate receptors: From the workbench to the bedside (2010, background): “…systemic treatment with MPEP or other mGlu5-receptor antagonists corrects most of the phenotypes associated with the lack of FMRP, including cognitive dysfunction, epileptic seizures, and morphological abnormalities (Yan et al., 2005; Tucker et al., 2006; Dölen et al., 2007; de Vrij et al., 2008).”
Common circuit defect of excitatory-inhibitory balance in mouse models of autism (2009, positive): “Rescue of ASD models, such as the FMR1 knockout mouse by mGluR5 manipulation [33], can then be reconsidered in terms of rebalancing PV-cell recruitment, as mGluR5 is essential for long-term potentiation of excitatory synapses onto these fast-spiking GABAergic neurons [34].”
The fragile X syndrome protein represses activity-dependent translation through CYFIP1, a new 4E-BP. (2008, methodology): “CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector”
Spatially restricting gene expression by local translation at synapses (2010, neutral): “For example, the Fmr1 KO mouse exhibits aberrant numbers and/or activity of mGluR5 [86,87], dopamine [88] and AMPA [89] receptor signaling.”
Fragile X Mental Retardation Protein Regulates New Neuron Differentiation in the Adult Olfactory Bulb (2011, background): “This is very interesting as dFmrp plays a role in activity-dependent axon pruning (Tessier and Broadie, 2008), and as Fmr1 KO mice display deficits in neocortical plasticity in response to sensory deprivation (Dölen et al., 2007; Bureau et al., 2008).”
Translational control of long-lasting synaptic plasticity and memory. (2009, positive): “The strongest evidence for a role of FMRP in mRNA repression is based on genetic models (flies and mice lacking FMRP) (Bolduc et al., 2008; Dolen et al., 2007).”